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DRUG:

REGN5093-M114

i
Other names: REGN5093-M114
Company:
Regeneron
Drug class:
Tubulin inhibitor, c-MET-targeted antibody-drug conjugate
Related drugs:
9ms
Study of REGN5093-M114 (METxMET Antibody-Drug Conjugate) in Adult Patients With Mesenchymal Epithelial Transition Factor (MET) Overexpressing Advanced Cancer (clinicaltrials.gov)
P1/2, N=237, Recruiting, Regeneron Pharmaceuticals | N=83 --> 237 | Trial completion date: Dec 2026 --> Feb 2030 | Trial primary completion date: Dec 2026 --> Feb 2030
Enrollment change • Trial completion date • Trial primary completion date • Metastases
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MET overexpression
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Libtayo (cemiplimab-rwlc) • REGN5093-M114
over1year
A Phase 1/2 Study of REGN5093-M114, a METxMET Antibody-Drug Conjugate, in Patients with MET-Overexpressing NSCLC (IASLC-WCLC 2023)
Currently, this study is enrolling patients. As of 30 March 2023 17 patients across the five dose levels (table 1).Dose Level (DL)Number of patients enrolledDL11DL23DL33DL44DL56
Clinical • P1/2 data
|
MET (MET proto-oncogene, receptor tyrosine kinase)
|
MET amplification • MET exon 14 mutation • MET overexpression
|
REGN5093-M114
2years
Preclinical • Journal
|
EGFR (Epidermal growth factor receptor) • MET (MET proto-oncogene, receptor tyrosine kinase) • PTEN (Phosphatase and tensin homolog)
|
EGFR mutation • MET amplification • EGFR overexpression • MET overexpression • MET mutation • MET expression • MET Y1230C
|
Tagrisso (osimertinib) • Orpathys (savolitinib) • REGN5093-M114
over2years
A MET targeting biparatopic antibody-drug conjugates (ADC), REGN5093-M114, has an antitumor efficacy in NSCLC harboring MET gene alterations (AACR 2022)
We evaluated the antitumor activity of REGN5093-M114 in patient-derived tumor xenograft (PDX) models from EGFR-mutant NSCLC patients with acquired resistance to osimertinib plus savolitinib, including acquired MET p.Y1230C mutation. Finally, we determined whether REGN5093-M114 is able to overcome acquired resistance to the MET-TKI, tepotinib, using PDC from METex14 mutant NSCLC patients. In acquired MET-amplified EGFR-TKI resistant PDCs, PDOs, ATCC cell lines and PDX models, REGN5093-M114 alone exhibited a significant antitumor efficacy compared to MET-TKI or the MET x MET biparatopic antibody (REGN5093), but had no effect on some models with same MET copy number as the sensitive models... REGN5093-M114 has the potential to be a novel therapeutic option in NSCLC harboring MET genetic alterations, and further clinical application is highly warranted.
Clinical • Late-breaking abstract
|
EGFR (Epidermal growth factor receptor) • MET (MET proto-oncogene, receptor tyrosine kinase) • PTEN (Phosphatase and tensin homolog)
|
EGFR mutation • MET amplification • EGFR overexpression • MET exon 14 mutation • MET overexpression • MET mutation • MET expression • MET Y1230C
|
Tagrisso (osimertinib) • Orpathys (savolitinib) • Tepmetko (tepotinib) • REGN5093-M114